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Disease Mechanisms > Ch 28: CNS > Flashcards

Ch 28: CNS Flashcards

1
Q

what makes up the central nervous system

A

brain and spinal cord

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2
Q

what makes up the peripheral nervous system

A

spinal and cranial nerves

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3
Q

what are the two main divisions of the PNS

A

sensory (afferent) division
motor (efferent) division

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4
Q

what are the two sensory divisions of the PNS

A

somatic (general & special)
visceral

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5
Q

what are the two motor divisions of the PNS

A

somatic
autonomic (visceral)

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6
Q

what are the two divisions of the visceral motor (autonomic nervous system)

A

parasympathetic
sympathetic

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7
Q

what are the principal functional unit of the CNS

A

neurons

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8
Q

what are neuroglial cells

A

provide structural support, protection, and maintain their environment

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9
Q

what are astrocytes

A

cell of the CNS
anchor neurons and blood vessels
facilitate the blood brain barrier
repair damaged tissue

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10
Q

what is an oligodendrocyte

A

cell of CNS
have extensions that wrap around a CNS axon and myelinate it

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11
Q

what is a microglial cell

A

cell of CNS
brain phagocyte

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12
Q

what is an ependymal cell

A

cell of CNS
line cavities
have cilia to circulate CSF
produce small amounts of CSF

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13
Q

what are schwann cells

A

cell of PNS
myelinate axons of PNS
repair damaged axons

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14
Q

what are satellite cells

A

cells of PNS
support cell bodies of PNS axons

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15
Q

what are the myelinating cells of the CNS

A

oligodendrocytes

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16
Q

what is the myelinating cell of the PNS

A

schwann cells

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17
Q

what is the purpose of myelination

A

to allow the action potiental to travel down the axon faster

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18
Q

what are the 5 main disorders of the nervous system

A

multiple sclerosis (MS)
creutzfeldt-jakob disease (CJD)
alzheimer (AD)
parkinson disease (PD)
amyotrophic lateral sclerosis (ALS)

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19
Q

what are some features of multiple sclerosis (MS)

A

demylination of CNS axons at distinct locations
causes scarring (sclerosis or plaque) which decreases neural transmission
patients can get better temporarily then get bad again once a different area is affected

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20
Q

what are the three gene mutations that can cause of multiple sclerosis (MS)

A

mutations in HLA-DR, IL2RA, and IL7RA

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21
Q

which mutated gene gives you a 3-fold risk of developing multiple sclerosis (MS)

A

HLA-DRB1*1501

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22
Q

what is the environmental factor that can cause multiple sclerosis (MS)

A

being away from the equator
likely cause is lack of vitamin D

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23
Q

what is the mechanism of multiple sclerosis (MS)

A

helpter T cells, cytotoxic T cells, and plasma B cells cross the blood brain barrier and enter the CNS
they cause an inflammatory response and kill oligodendrocytes which leads to demyelination and axon degeneration
eventually, we get neuron death and brain atrophy

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24
Q

how do helper T 1 cells play a role in multiple sclerosis (MS)

A

they release IFN-y which leads to macrophage activation

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25
Q

how do helper T 17 cells play a role in multiple sclerosis (MS)

A

they release IL17 and IL22 which causes recruitment of leukocytes

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26
Q

who is most at risk for multiple sclerosis and when are they typically diagnosed

A

most common in women
usually diagnosed between 20-40 yrs

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27
Q

how does multiple sclerosis (MS) affect the optic nerve

A

damage of optic nerve leads to optic neuritis (inflammation of optic nerve)

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28
Q

how does multiple sclerosis (MS) affect the brainstem

A

damage of brainstem leads to ataxia (loss of cordination) and nystagmus (uncontrolled eye movements)

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29
Q

how does multiple sclerosis affect (MS) the spinal cord

A

damage of spinal cord leads to motor and sensory impariment, spasticity (stiff muscles), and loss of bladder control

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30
Q

what are evoked potentials

A

a type of diagnostic test for multiple sclerosis
electrodes stimulate neurons to test their activity

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31
Q

what are oligoclonal bands

A

a diagnostic test of multiple sclerosis (MS)
spinal tap is performed to get CSF
it’s run using electrophoresis
looking for oligoclonal bands (IgG) in CSF which would indicated MS

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32
Q

how is an MRI used for multiple sclerosis (MS)

A

MRIs are used to look for white matter plaques cause by demyelination

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33
Q

what are the three diagnostic tests of multiple sclerosis (MS)

A

evoked potentials
oligoclonal bands in CSF
MRI

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34
Q

what are the three main treatments of multiple sclerosis (MS)

A

corticosteroids
interferon beta
specific medications

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35
Q

what are the two corticosteroids used to treat acute multiple sclerosis (MS)

A

prednisone
cortisone

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36
Q

how do corticosteroids help treat multiple slcerosis (MS)

A

shorten recovery period after acute attack
helps to restore blood brain barrier
blocks some of the macrophage and lymphocyte activity to stop demylination

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37
Q

how does interferon beta treat multiple sclerosis (MS)

A

affects the function of APCs, T cells, and B cells (plasma cells)

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38
Q

what is the definition of a neurodegenerative disease

A

disease caused by an accumulation of protein aggregates which leads to progressive loss of neurons

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39
Q

neurogenerative diseases that cause cognitive changes affect which areas of the brain

A

cerebral cortex and hippocampus
ex. alzheimer disease

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40
Q

neurogenerative diseases that cause movement disorders affect which area of the brain

A

basal ganglia
ex. parkinson disease

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41
Q

neurogenerative diseases that cause limb weakness and difficulty swallowing and breathing affect which area of the brain

A

spinal cord
ex. amyotrophic lateral sclerosis (ALS)

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42
Q

what is the most common demyelinating disorder

A

multiple sclerosis (MS)

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43
Q

what are prion diseases

A

rapidly progressing neurodegenerative diseases that lead to progressive dementia
ex. CJD

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44
Q

what are normal prion proteins

A

PrPC
cytoplasmic proteins found in all cells but mostly neurons and glial cells

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45
Q

what is the mechanism of a prion disease

A

normal prion proteins (PrPC) undergo misfolding and become (PrPSC)
misfolded prion proteins (PrPSC) are protease resistant and accumulate in the neuronal tissue
causes fatal white matter damage

46
Q

what are the three ways to get a prion disease

A

sporadicly (randomly)
familial (mutation)
transmitted (inoculation or ingestion)

47
Q

what is the most common prion disease

A

creutzfeldt-jakob disease (CJD)

48
Q

which age range is most affected by creutzfeldt-jakob disease

A

60-70 years old

49
Q

what are the three ways to get creutzfeldt-jakob disease (CJD)

A

sporadic (randomly)
familial (mutations)
iatrogenic (procedure)

50
Q

what is the most common way to get creutzfeldt-jakob disease (CJD)

A

sporadic (90%) - randomly

51
Q

what is the familial cause of creutzfeldt-jakob disease (CJD)

A

mutation in PRNP that encodes for misfolded prion proteins

52
Q

what are the three iatrogenic causes of creutzfeldt-jakob disease (CJD)

A

transplant - corneal/dural
implantation of brain electrodes
contaminated cadaveris hGH (human growth hormone)

53
Q

what are four symptoms of creutzfeldt-jakob disease (CJD)

A

behavior changes
dementia
involuntary muscle jerking
brain shrinkage

54
Q

typically, how long does someone with creutzfeldt-jakob disease (CJD) live

A

7 months

55
Q

what is the most common form of dementia in adults older than 60

A

alzheimer disease

56
Q

what are the two major types of alzheimer disease

A

familial (early-onset) - mutation
sporadic - random

57
Q

what is the most common type of alzheimer disease

A

sporadic (90%) - random

58
Q

what are the two prominant features of Alzheimer disease

A

extracellular amyloid-beta (AB) plaques
intracellular neurofibrillary (tau) tangles

59
Q

explain the mechanism of alzheimer disease

A

amyloid precursor protein is cut at beta-secretase site instead of normal alpha-secretase site
after gamma-secretase cleaves its spot (the same in both pathways), we’re left with an alphabeta monomer which is highly prone to aggregation
aggregation of these monomers leads to amyloid fibrils which causes plaques and tangles, ultimately leading to neuronal damage

60
Q

explain briefly how Tau tangles are formed in Alheimer disease

A

creation of alphabeta monomor activates kinases that lead to Tau phosphorylation
Tau phosphorylation leads to Tau aggregates
Tau aggregates lead to plaques and tangles that and cause neuronal damage

61
Q

what are the three familial causes of alzheimer disease

A

amyloid precursor protein (APP gene)
presenilin 1 (PSEN1 gene)
presenilin 2 (PSEN2 gene)

62
Q

what chromosome is the amyloid precursor protein (APP gene) on

A

chromosome 21

63
Q

how is down syndrome releated to alzheimer disease

A

those with down syndrome have three copies of chromsome 21
if all three of those copies possess a amyloid precursor protein (APP) gene mutation, it increases their risk for developing Alzheimer disease

64
Q

what two factors are important for the sporadic form of Alzheimer disease

A

interactions among genetic and environmental factors

65
Q

which three environmental factors can cause alzheimer disease

A

aluminum in drinking water
large levels of electromaganetic fields
exposure to solvents/pesticides

66
Q

which genetic factor can lead to the sporadic form of alzheimer disease

A

mutation in apolipoprotein E (apoEA) on chromosome 19

67
Q

what are six symptoms of alzheimer disease

A

memory disturbances
language deficits
loss of math skills
loss of learned motor skills
mute
inability to walk

68
Q

what are the four ways to test for alzheimer disease

A

exclusion
MRI
mini mental state exam (MMSE)
post-mortem exam

69
Q

which two things would be seen on a MRI in an alzheimer patient

A

brain atrophy
enlarged ventricles

70
Q

what two things are seen on a post-mortem exam in a patient with alzheimer

A

widened sulci and thin gyri of temporal and frontal lobes
definitive diagnostic tool

71
Q

what are three things used to treat alzheimer disease

A

cholinesterase inhibitors
antipsychotics/mood stabilizers
cognitive stimulation therapy

72
Q

when are cholinesterase inhibitors most effective in treating alzheimer disease

A

mild disease states: 6-12 months

73
Q

what is the average lifespan of someone with alzheimers after diagnosis

A

8 years

74
Q

what is the main function of the basal ganglia

A

controls movement to ensure it is smooth

75
Q

what are the three pathways the basal ganglia influence

A

direct pathway
indirect pathway
nigrostriatal pathway

76
Q

what is the direct pathway

A

increases motor function - movement
increased further by dopamine

77
Q

what are the four areas involved in the direct pathway

A

cortex
striatum
globus pallidus internus
thalamus

78
Q

what is the indirect pathway

A

decreases motor function - no movement
inhibited further by dopamine

79
Q

what are the six areas involved in the indirect pathway

A

cortex
striatum
globus pallidus externus
globus pallidus internus
thalamus
substantia nigra

80
Q

what is the nigrostriatal pathway

A

purely excitatory pathway
influences both pathways to help control movement

81
Q

what is parkinson disease

A

degenerative disorder of basal ganglia

82
Q

what is the mechanism of parkinson disease

A

accumulation of protein aggregates cause destruction of dopaminergic neurons from substantia nigra
less SN neurons means less dopamine
less dopamine means less inhibiting of D2 pathway and less stimulating D1 pathway
causes overall reduction in movement

83
Q

what are the two causes of primary parkinsonism

A

mostly idiopathic - unknown
familial - inherited

84
Q

what are the four causes of secondary parkinsonism

A

drug induced
encephalitis
trauma
other neurodegenerative disorders

85
Q

what is the environmental toxin that can cause parkinson disease

A

MPTP
used for animal studies but can be accidentally taken by humans too

86
Q

15% of those with parkinson disease have what

A

a first-degree relative who also has the disease

87
Q

what are the two gene mutations that can lead to parkinson disease

A

LRRK2 (PARK8)
SNCA

88
Q

how does mutation in LRRK2 (PARK8) gene cause parkinson disease

A

dominant mutation that encodes for dardarin protein
causes gain of function

89
Q

how does mutation in SNCA gene cause parkinson disease

A

encodes for alpha-synuclein
expressed mostly in the substantia nigra
forms aggregates which are toxic to neurons

90
Q

what is a major component of Lewy bodies

A

alpha-synuclein

91
Q

what are the six major symptoms of parkinson disease

A

resting tremor
mask-like face (no emotions)
rigidity
postural instability
bradykinesia (slow movement)
flexed joints

92
Q

what is amyotrophic lateral sclerosis (ALS)

A

aka lou gehrig disease
degeneration of upper and/or lower motor neurons

93
Q

which age range is at most risk of developing amyotrophic lateral sclerosis (ALS)

A

mostly men between 40-70 years

94
Q

what are six possible causes of sporadic amyotrophic lateral sclerosis (ALS)

A

excessive glutamate
immune disturbances
apoptotic factors
viruses
heavy metals
enzyme abnormalities

95
Q

what two factors are needed to cause sporadic amyotrophic lateral sclerosis (ALS)

A

genetic and environmental factors

96
Q

what are three mutations that can lead to familial amyotrophic lateral sclerosis (ALS)

A

hexanucleotide repeat expansion in C9orf72
superoxide dismutase 1 (SOD-1)
SPTLC1

97
Q

how does a mutation in C9orf72 lead to familial amyotrophic lateral sclerosis (ALS)

A

dominant, expanded repeats that causes neuronal deposits (TDP-43 inclusions)

98
Q

which gene is most responsible for familial amyotrophic lateral sclerosis (ALS)

A

C9orf72 (40%)

99
Q

how does a mutation in superoxide dismutase 1 lead to familial amyotrophic lateral sclerosis (ALS)

A

dominant mutation that causes a misfolded protein to aggregate
aggregation leads to apoptosis of neurons

100
Q

how do mutations in SPTLC1 lead to familial amyotrophic lateral sclerosis (ALS)

A

dominant mutation of protein coding gene
affects mostly children 4 and up - juvenile ALS

101
Q

mutation of which gene leads to juvenile, familal amyotrophic lateral sclerosis (ALS)

A

mutation in SPTLC1

102
Q

what is guamanian amyotrophic lateral sclerosis (ALS)

A

type of amyotrophic lateral sclerosis caused by neurotoxin in seed of diet

103
Q

what is the neurotoxin that is believed to cause guamanian amyotrophic lateral sclerosis (ALS)

A

BMAA

104
Q

what are the two unique symptoms of guamanian amyotrophic lateral sclerosis (ALS)

A

dementia
parkinson like symptoms

105
Q

what is the main symptom of amyotrophic lateral sclerosis (ALS)

A

loss of lower and upper motor neurons

106
Q

what are the four symptoms of loss of lower motor neurons in amyotrophic lateral sclerosis (ALS) patients

A

denervation of muscles
muscle atrophy
weakness
fasciculations (muscle twitches)

107
Q

what are the three symptoms of loss of upper motor neurons in amyotrophic lateral sclerosis (ALS) patients

A

paresis (weakness)
hyperreflexia
spasticity (stiff muscles)

108
Q

what is the life expectancy of someone with amyotrophic lateral sclerosis (ALS)

A

3 to 5 years after diagnosis

109
Q

what ultimately kills someone with amyotrophic lateral sclerosis (ALS)

A

paralysis of diaphragm and respiratory infection

110
Q

what are the two drugs used to slow progression of amyotrophic lateral sclerosis (ALS)

A

rilutek (riluzole)
antioxidant vitamins

111
Q

what are three antioxidant vitamins used to slow progression of amyotrophic lateral sclerosis (ALS)

A

vitamin E
vitamin C
beta-carotene

112
Q

what are the three things used to treat symptoms of amyotrophic lateral sclerosis (ALS)

A

NSAIDS for pain
baclofen (stiffness)
tizanidine (stiffness)

Disease Mechanisms (19 decks)

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